Lobbezoo F, Soucy J P, Hartman N G, Montplaisir J Y, Lavigne G J
Faculté de Médecine Dentaire, Université de Montréal, Québec, Canada.
J Dent Res. 1997 Sep;76(9):1610-4. doi: 10.1177/00220345970760091401.
An altered dopamine receptor status has been associated with sleep bruxism. Evidence from a functional neuro-imaging study has implicated an abnormal side imbalance in striatal D2 receptor expression in its pathophysiology. To assess the significance of this finding, we studied the effects of short-term administration of the preferential dopamine D2 receptor agonist bromocriptine on sleep bruxism in a double-blind, placebo-controlled polysomnographic and neuro-imaging study with a single crossover design. Six otherwise healthy and drug-free patients with sleep bruxism were entered into the trial. One of the patients dropped out due to an intercurrent illness, while three others were discontinued from the study due to severe adverse reactions to bromocriptine. Because of the high frequency and intensity of the side-effects, the trial was interrupted. Two patients, however, completed the trial without any adverse reactions. Their outcome measures are presented as single-patient clinical trials. Following a two-week administration of bromocriptine, both patients showed a decrease in the number of bruxism episodes per hour of sleep of about 20% to 30% with respect to the placebo. WHile no significant differences between both conditions (i.e., placebo and bromocriptine) were found for the number of bruxism bursts per episode, significantly lower root-mean-squared EMG levels per bruxism burst occurred during bromocriptine use. In association with this polysomnographically established attenuation of sleep bruxism, bromocriptine afforded a decreased normal side distribution of striatal D2 receptor binding, as was evidenced by single-photon-emission computed tomography using the radioactive D2 receptor antagonist iodine-123-iodobenzamide. This study supports previous suggestions that the central dopaminergic system may be involved in the modulation of sleep bruxism. To see if the present findings apply across a population, investigators should use a peripheral D-2 antagonist to prevent side-effects.
多巴胺受体状态改变与睡眠磨牙症有关。一项功能性神经影像学研究的证据表明，纹状体D2受体表达的异常侧失衡在其病理生理学中起作用。为了评估这一发现的意义，我们在一项采用单交叉设计的双盲、安慰剂对照多导睡眠图和神经影像学研究中，研究了短期给予多巴胺D2受体激动剂溴隐亭对睡眠磨牙症的影响。六名无其他疾病且未服用药物的睡眠磨牙症患者进入试验。其中一名患者因并发疾病退出，另外三名患者因对溴隐亭有严重不良反应而退出研究。由于副作用的高频率和高强度，试验中断。然而，两名患者完成了试验且无任何不良反应。他们的结果测量以单患者临床试验形式呈现。在给予溴隐亭两周后，与安慰剂相比，两名患者每小时睡眠中的磨牙发作次数均减少了约20%至30%。虽然两种情况（即安慰剂和溴隐亭）下每次发作的磨牙阵发次数没有显著差异，但在使用溴隐亭期间，每次磨牙阵发的肌电图均方根水平显著降低。与多导睡眠图确定的睡眠磨牙症减轻相关，溴隐亭使纹状体D2受体结合的正常侧分布减少，使用放射性D2受体拮抗剂碘-123-碘苄胺的单光子发射计算机断层扫描证明了这一点。本研究支持先前的观点，即中枢多巴胺能系统可能参与睡眠磨牙症的调节。为了确定目前的发现是否适用于整个人群，研究人员应使用外周D - 2拮抗剂来预防副作用。
